March 30, 2015

New issue: March 30th 2015

In the latest issue of JCB, Coon et al. reveal how the adhesion molecule VE-cadherin allows endothelial cells to respond to fluid shear stress. As explained in this week’s In Focus, the researchers find that the transmembrane domain of VE-cadherin binds to the transmembrane domains of the growth factor receptors VEGFR2 and VEGFR3, recruiting them into a mechanosensory complex at endothelial cell junctions.

Somasekharan et al. show that stress granules – cytoplasmic particles that store mRNAs when cells are under duress – can promote tumor metastasis. As summarized here, the researchers show that a protein called YB-1 stimulates stress granule assembly by promoting translation of a stress granule protein called G3BP1, and cancer cells lacking G3BP1 are less able to metastasize in vivo.

Moudgil et al. report that the mitotic checkpoint protein Spindly must be farnesylated at its C-terminus in order to be recruited to kinetochores. Farnesylation promotes Spindly’s association with the RZZ complex, and blocking this lipid modification inhibits Spindly’s localization to kinetochores, delaying mitotic cells’ progression through prometaphase. More here.

Elsewhere, West et al. describe how recycling endosomes control synaptic growth in a Drosophila model of frontotemporal dementia (summary here), and, in the latest of our 60th anniversary From The Archive articles, we remember when Narendra et al. demonstrated how a protein linked to Parkinson’s disease regulates mitochondrial homeostasis.

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